Previous findings suggest that cardiac muscle responds quite differently to various programs of exercise and/or myocardial stress. Swimming and sprint-type running produce increases in ATPase activity of the contractile proteins, which could enhance myocardial functional capacity. Prolonged endurance running produces relatively litte change on this system even though the animals become highly trained. In contrast, pressure overload causes reduced actomyosin ATPase activity and a reduced functional capacity of the heart. The factor(s) regulating these contrasting responses are unknown, but could involve different degrees of sympathetic activity affecting the heart under different conditions of stress. A series of experiments is proposed to test the effects of chemical sympathectomy and of experimental conditions to alter potential sympathetic activity in mediating potential cardiac muscle changes of rats in response to physical activity including: (1) swimming; (2) treadmill running; (3) pressure overload combined with exercise; and (4) chronic exercise with a reduced capacity for venous return. Experimental groups (normal, sympathectomized, thyroid deficient, and normal Beta blockade) will be subjected to the above conditions for eight weeks and measurements will be performed on: (a) myosin ATPase properties; (b) sarcoplasmic reticulum (FSR) calcium uptake properties; and (c) cardiac functional parameters of pressure development and cardiac output. These experiments will more clearly define the need for intact sympathetic and/or thyroid function in mediating certain cardiac adaptations to chronic exercise.